Transendothelial Migration of Myeloma Cells Is Increased by Tumor Necrosis Factor (TNF)-α <b>
                     <i>via</i>
                  </b> TNF Receptor 2 and Autocrine Up-Regulation of MCP-1

Jöhrer, Karin; Janke, Katrin; Krugmann, Jens; Fiegl, Michael; Greil, Richard

doi:10.1158/1078-0432.ccr-1053-03

Cited by 74 publications

(53 citation statements)

References 40 publications

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“…These findings suggest that exosomes may selectively transfer certain proteins to the recipients cells, behaving as vesicles that selectively transport specific proteins to cells they interact with ( Figure 7A). It was previously reported that CCL2 plays a crucial role in MM pathogenesis and disease progression, demonstrated both in vitro and in vivo (41,42). Our present findings also demonstrated that MM BM-MSC-derived exosomes contain higher levels of CCL2 than do normal BM-MSC-derived exosomes, confirming the role of this protein in supporting MM biology.…”

Section: Figuresupporting

confidence: 87%

BM mesenchymal stromal cell–derived exosomes facilitate multiple myeloma progression

et al. 2013

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BM mesenchymal stromal cells (BM-MSCs IntroductionThe BM microenvironment plays a crucial role in multiple myeloma (MM) pathogenesis by supporting plasma cell growth, survival, and drug resistance, which has been partially attributed to the ability of MM BM mesenchymal stromal cells (BM-MSCs) to secrete growth factors and cytokines such as IL-6, IGF-1, VEGF, and many others (1-3). These observations are indicative of paracrine growth circuits between BM-MSCs and clonal plasma cells and vice versa, which suggests that the BM niche provides an optimal substrate for MM cell localization and growth. Nevertheless, little is known about the putative mechanisms by which the BM microenvironment can lead to initiation or progression of oncogenesis in this disease.It was recently reported that cell-cell communication is mediated by exosomes. Exosomes are small nanometer-sized (50-100 nm) vesicles of endocytic origin that are released in the extracellular milieu by several cell types (4-11) under physiological and pathological conditions, including antigen presentation, transmission of infectious agents, and tumors (12, 13). The role of exosomes in tumor progression is due to the ability of tumor cell-derived exosomes to modulate and mold the host microenvironment, thereby promoting tumor cell growth and disease progression (14-17).

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Section: Figuresupporting

confidence: 87%

BM mesenchymal stromal cell–derived exosomes facilitate multiple myeloma progression

et al. 2013

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“…It is reported that activation of TNFR2 in skin tumors could promote proliferation of tumor cells, not induce apoptosis (12). Tanimura et al (11) reported that TNF-α could promote invasiveness of cholangiocarcinoma cells via TNFR2 and Jöhrer et al (13) reported that TNFR2 was required for migration of myeloma cells induced by TNF-α. However, the studies by Arnott et al, Baud and Karin, and Grell et al (14)(15)(16) reported that, regardless of DD, TNFR2 could also activate death signals and induce cell death by ligand passing to TNFR1.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor receptor 2 promotes growth of colorectal cancer via the PI3K/AKT signaling pathway

Zhao

Liu

2016

Oncology Letters

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Abstract. Tumor necrosis factor receptor 2 (TNFR2) is the receptor for tumor necrosis factor α (TNF-α). TNFR2 differs from tumor necrosis factor 1 (TNFR1) in various ways and is mainly expressed in hematopoietic and endothelial cells. However, studies about its functions in tumors are limited. The contributions of TNFR2 in colorectal cancer (CRC) remain unknown. In the present study, it was found that TNFR2 was positively associated with Ki67 expression in CRC tissues using immunohistochemistry (IHC), and western blot analysis found that Ki67 was upregulated by overexpressing TNFR2 in SW1116 cells and inhibited by silencing TNFR2 in HT29 cells. Methyl thiazolyl tetrazolium assay found that growth of SW1116 cells overexpressing TNFR2 was significantly increased compared with the control group and that the growth of HT29 cells subsequent to silencing TNFR2 was significantly decreased compared with the control group. Clone formation assay found that more clones were formed in SW1116 cells overexpressing TNFR2 than the control group, and less clones formed in HT29 cells subsequent to silencing TNFR2 than the control group. In addition, western blot analysis found that phosphorylation of protein kinase B (AKT) was activated subsequent to overexpressing TNFR2 in SW1116 cells, and inhibited following silencing of TNFR2 in HT29 cells. Additionally, treatment using LY294002 significantly abrogated the promotion of Ki67 expression, growth and clone formation abilities induced by TNFR2 overexpression in SW1116 cells. All the results suggest that TNFR2 can significantly promote CRC growth via the phosphoinositide 3-kinase/AKT signaling pathway; this provides evidential support for taking TNFR2 as a new target for CRC treatment.

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“…1 Several cytokines that are involved in the pathogenesis of MM disease, such as IGF-1, tumor necrosis factor (TNF)-α, vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF)-2 and SDF-1α, promote MM cell migration. [2][3][4][5][6] The 68 kDa glycoprotein HGF, produced by stromal cells in the BM, is a pleiotropic cytokine with mitogenic, motogenic and morphogenic properties. 7 The HGF receptor c-Met is a tyrosine kinase type receptor.…”

Section: Introductionmentioning

confidence: 99%

Hepatocyte growth factor promotes migration of human myeloma cells

Holt¹,

Fagerli²,

Baykov³

et al. 2008

Haematologica

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Multiple myeloma is characterized by the accumulation and dissemination of malignant plasma cells in the bone marrow. Cell migration is thought to be important for these events. We studied migration in a Transwell two-chamber assay and tested the motogenic effect of various cytokines. In addition to insulin-like growth factor-1 and stromal cell-derived growth factor-1α, previously known as chemoattractants for myeloma cells, we identified hepatocyte growth factor as a potent attractant for myeloma cells. Hepatocyte growth factor-mediated migration was dependent on phosphatidylinositol-3-kinase, involved the MAPK/Erk signaling cascade and VLA-4 integrins, but did not involve Akt, mTOR or G proteins.

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Transendothelial Migration of Myeloma Cells Is Increased by Tumor Necrosis Factor (TNF)-α via TNF Receptor 2 and Autocrine Up-Regulation of MCP-1

Cited by 74 publications

References 40 publications

BM mesenchymal stromal cell–derived exosomes facilitate multiple myeloma progression

BM mesenchymal stromal cell–derived exosomes facilitate multiple myeloma progression

Tumor necrosis factor receptor 2 promotes growth of colorectal cancer via the PI3K/AKT signaling pathway

Hepatocyte growth factor promotes migration of human myeloma cells

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